Related Experiment Video
Updated: Aug 11, 2026

A Rat Model of Middle Cerebral Artery Occlusion/Reperfusion Without Damaging the Anatomical Structure of Cerebral Vessels
Published on: May 17, 2024
Expression of heme oxygenase-1 protein and messenger RNA in permanent cerebral ischemia in rats
Rong Fu1, Zhong Qiu Zhao, Hong Yang Zhao
1Neurosurgery Department, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. furongLP@yahoo.com.cn
Background:
Carbon monoxide has been regarded as a gaseous molecular messenger like nitric oxide.
Purpose:
To clarify the role of heme oxygenase-1 in the permanent cerebral ischemia at the protein and mRNA level.
Methods:
The expression of heme oxygenase-1 protein and messenger RNA was investigated at different time points following MCAO using immunohistochemistry, Western blotting, RT-PCR, and Northern blotting.
Results:
Increased HO 1immunoreactivity was detected in hippocampal and cortical neurons after 1 hour of ischemia, and was also observed in astroglial cells. After 12 hours of ischemia, HO-1 was found in both neurons and glia in cerebral cortex and thalamus, and in striatal glia cells. Western blotting analysis show the expression of HO-1 protein in cortical neurons reached the peak after 12 hours of occlusion and decreased gradually, but was still detected at day 7 post-occlusion. The expression of messenger RNA was examined in the brains of rats subjected to permanent cerebral ischemia by semi-quantitative RT-PCR and Northern blotting. HO-1 mRNA transcription could be detected 1 hour after occlusion. After 1 to 6 hours of occlusion, the expression of HO-1 rose rapidly, reaching a peak at 12 hours post-occlusion, decreased gradually, and lasted until day 7 of occlusion. Although HO activity of cerebral tissue can be detected in both sham-operated group and operated groups, the HO activity in operated groups is much stronger than that in sham-operated group.
Conclusions:
The induction of HO-1 protein may protect cerebral tissues from ischemic damage.
